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Biomedical subjects

I Goldstein

Publications and source records attributed to I Goldstein.

At least 271 records · Page 15Linked to original sources

Effects of expiratory threshold loading during steady-state exercise.

Increases in functional residual capacity (FRC) decrease inspiratory muscle efficiency; the present experiments were designed to determine the effect of FRC change on the ventilatory response to exercise. Six well-trained adults were exposed to expiratory threshold loads (ETL) ranging from 5 to 40 cmH2O during steady-state exercise on a bicycle ergometer at 40-95% VO2max. Inspiratory capacity (IC) was measured and changes of IC interpreted as changes of FRC. ETL did not consistently limit exercise performance. At heavy work (greater than 92% VO2max) minute ventilation decreased with increasing ETL; at moderate work (less than 58% VO2max) it did not. Decreases in ventilation were due to decreases in respiratory frequency with prolongation of the duration of expiration being the most consistent change in breathing pattern. At moderate work levels, FRC increased with ETL; at maximum work it did not. Changes in FRC were dictated by constancy of tidal volume and a fixed maximum end-inspiratory volume of 80-90% of the inspiratory capacity. When tidal volume was such that end-inspiratory volume was less than this value, FRC increased with ETL. Mouth pressure measured during the first 0-1 s of inspiratory effort against an occluded airway (P0-1) was increased by ETL equals 30 cmH2O, in spite of the fact that ventilation was decreased. We concluded that changes in FRC due to ETL had no effect on the ventilatory response to exercise and that changes in P0-1 induced by ETL did not reflect changes of inspiratory drive so much as changes of the pattern of inspiration.

Adult↗

Action of group A streptococcus extracellular product(s) on the connective tissue of the bovine heart valve.

Group A streptococcal strains isolated from rheumatic fever patients were cultivated in the presence of bovine heart valves in a medium devoid of components from animal origin. Other group A streptococci and various bacteria were used as controls. The supernatant of these cultures was extracted and analyzed chemically and immunologically. The extracts prepared from cultures of two "rheumatogenic" strains in the presence of bovine heart valves showed fraction(s) containing proteins, oses (neutral and amined), and uronic and sialic acids. This fraction(s) was immunologically active with both anti-group A streptococcus and antisoluble connective glycoprotein antisera, with a partial identity reaction. Experiments with a diffusion chamber and attempts to precipitate a postulated enzyme from the culture of these strains by ammonium sulfate suggest that this action is due to an extracellular product of the bacteria. The meaning of these data in the physiopathology of rheumatic cardiac lesions is briefly discussed.

Amino Acids↗

Mechanisms of lysosomal enzyme release from human leukocytes: microtubule assembly and membrane fusion induced by a component of complement.

A low-molecular-weight component of complement, similar to or identical with human C5a, interacts with human polymorphonuclear leukocytes treated with cytochalasin B and provokes extracellular release of lysosomal enzymes from these cells. Enzyme release occurs in the absence of particles and is selective in that it is not accompained by release of cytoplasmic enzymes. Cell viability is not altered. Pharmacologic agents that regulate secretion of other inflammatory mediators influenced complement-dependent enzyme release: cAMP and theophylline, prostaglandin E(1) and colchicine inhibited, whereas cGMP enhanced release of enzymes. Ultra-structural histochemistry of cells exposed to this component of complement revealed degranulation, fusion of lysosomal with plasma membranes, and transient assembly of microtubules associated with the release of endogenous myeloperoxidase. Our findings suggest that these intracellular events are common to two important responses of polymorphonuclear leukocytes in inflammation and tissue injury: (a) release of lysosomal hydrolases and (b) chemotaxis.

Chemotaxis↗